Abstract
PAF-acether is a phospholipid synthesized by most animal tissues and exerting a strong decrease on the heart's contractile force and coronary flow. PAF-acether (10(-9) and 10(-10)M) was administered to isolated guinea pig hearts perfused via the Langendorff apparatus with Chenoweth solution. Zinc (1.5 microM) is known to benefit heart function thus, Zn2+ (1.5, 7.5, and 30 microM) was added in the perfusing solution before or after PAF-acether administration. Contractile force, coronary flow, and heart rate were recorded by means of a Narco MK-IV Physiograph throughout all modes of perfusion. Calcium inhibitor (Verapamil 10(-10)M) and Pb+2 Co2+ (1.5 x 10(-6)M) were used subsequently in the perfusing solutions in order to elucidate some of the Zn and PAF interactions observed. All hearts were analyzed for their Zn and Ca content by means of an Atomic Absorption Spectrophotometry (AAS). Our data suggest that low concentrations of zinc (1.5 microM) can strongly inhibit PAF-induced decrease of contractile force and coronary flow. Zinc-inhibiting effects on PAF's negative inotropic action (myocytic level) is not exerted through Zn-Ca antagonism. Nevertheless, a Zn-Ca antagonism in the arteriolar level cannot be excluded. Zinc inhibits PAF selectively only if it is administered before PAF injection and this strongly suggests a receptor interaction between the metal and the phospholipid at the heart level.
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